Plasma p-tau217 as a suitable biomarker for monitoring cognitive changes in Alzheimer’s disease - Poster presentation - Abstract & results

Sep 30, 2026

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Background: After approval of anti-amyloid therapies in Alzheimer’s disease (AD), surrogate biomarkers are needed to track treatment effects that translate into clinical benefits. Candidate markers—amyloid-PET, tauPET, plasma phosphorylated tau (p-tau), and MRI-assessed atrophy—capture key pathophysiological changes, but longitudinal change rates may better reflect disease dynamics. Therefore, the study identified which biomarker most effectively tracks cognitive change, supporting efficient monitoring of disease-modifying treatments. Method: ADNI and A4 longitudinal cohorts were analyzed using mixed and linear models.

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DOI: 10. 1002/alz70856_104771 BIOMARKERS POSTER PRESENTATION BIOMARKERS (NON-NEUROIMAGING) Plasma p-tau217 as a suitable biomarker for monitoring cognitive changes in Alzheimer’s disease Davina Biel 1 Anna Steward 1 Anna Dewenter 1 Amir Dehsarvi 1 Sebastian Roemer-Cassiano 1 Lukas Frontzkowski 1, 2 Fabian Hirsch 1 Zeyu Zhu 1 Matthias Brendel2, 3, 4 Nicolai Franzmeier4, 5, 6 1 Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Bavaria, Germany 2 Department of Nuclear Medicine, University Hospital, LMU Munich, Munich, Bavaria, Germany 3 German Center for Neurodegenerative Diseases (DZNE), Munich, Germany 4 Munich Cluster for Systems Neurology (SyNergy), Munich, Bavaria, Germany 5 University of Gothenburg, The Sahlgrenska Academy, Institute of Neuroscience and Physiology, Psychiatry and Neurochemistry, Gothenburg, Sweden 6 Institute for Stroke and Dementia Research (ISD), LMU University Hospital, LMU, Munich, Bavaria, Germany Correspondence Nicolai Franzmeier, Munich Cluster for Systems Neurology (SyNergy), Munich, Bavaria, Germany. Email: [Nicolai.Franzmeier@med.uni-muenchen.de](Nicolai.Franzmeier@med.uni-muenchen.de) Abstract Background: With the approval of anti-amyloid therapies in Alzheimer’s disease (AD), surrogate biomarkers are urgently needed to monitor treatment effects that translate into clinical benefits. Candidate biomarkers, including amyloid-PET, tauPET, plasma phosphorylated tau (p-tau), and MRI-assessed atrophy, capture core pathophysiological changes in AD. While cross-sectional biomarker assessments are critical for diagnosis and staging, biomarker change rates may better reflect disease dynamics, making them more suitable for monitoring treatment efficacy. Therefore, we determined which biomarker most effectively tracks cognitive changes in AD, identifying those best suited for efficient monitoring of disease-modifying treatments. Method: We leveraged ADNI (N = 108) and A4 (N = 151) participants with longitudinal AD biomarker data (global amyloid-PET, temporal meta tau-PET, plasma p-tau217 , MRI-assessed cortical thickness in the AD signature region) together with cognitive assessments (ADNI: MMSE, ADAS13, CDR-SB; A4: MMSE, PACC). Linear mixed models were used to calculate change rates for biomarkers and cognition. To test whether biomarker changes track cognitive decline, linear models were applied, to test biomarker change rates as a predictor of cognitive change rates. Standardized beta values from bootstrapped linear models were extracted to compare the strengths of correlations between biomarkers and cognitive decline. For nonparametric comparisons, 95% confidence intervals (CIs) of standardized beta values were compared. Models were controlledforage, sex, education, and baseline cognition, with ADNI models additionally adjusted for clinical status. Result: In both cohorts, changes in temporal tau-PET, plasma p-tau217 , and MRIassessed cortical thickness were associated with cognitive decline (ADNI: Figure 1; A4: Figure 2). Amyloid-PET changes showed no significant association with cognitive changes (ADNI: Figure 1A+F+K; A4: Figure 2A+F). Bootstrapping confirmed that This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2025 The Alzheimer’s Association. Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association. Alzheimer’s Dement. 2025;21(Suppl. 2):e104771. [https://doi.org/10.1002/alz70856_104771](https://doi.org/10.1002/alz70856_104771) wi[leyonlinelibrary.com/journal/alz](leyonlinelibrary.com/journal/alz) 1of4 BIOMARKERS tau-PET, plasma p-tau217 , and cortical thickness track cognitive decline, but not amyloid-PET (ADNI: Figure 1E+J+O; A4: Figure 2E+J). Overlapping CIs for tau-PET and plasma p-tau217 indicated compara

FAQs

Which biomarkers were compared for tracking cognitive changes in Alzheimer’s disease?

The study compared global amyloid-PET, temporal tau-PET, plasma p-tau217, and MRI-assessed cortical thickness, alongside cognitive measures in ADNI and A4.

Did amyloid-PET changes relate to cognitive decline?

No. Changes in amyloid-PET showed no significant association with cognitive changes in both cohorts.

Why are tau-PET and plasma p-tau217 considered suitable monitoring biomarkers?

Both tau-PET and plasma p-tau217 changes were associated with cognitive decline, and overlapping confidence intervals suggested comparable predictive accuracy, with plasma p-tau217 offering a scalable clinical alternative.

Sep 30, 2026

Uploaded by Fahsai